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Why Beef Liver Pt. 2: Do we have the CUre?

In the first part of the “Why Beef Liver?” series we mainly focused on iron, and how it affects the mitochondria, leads to loss of normal cellular respiration, and is ultimately associated with an increase in chronic disease. The question begs however, what does this all have to do with beef liver? After all, doesn’t beef liver contain iron as well? The answer to the former question is unequivocally, a lot. The answer to the latter is that iron in itself is not a bad thing. Iron is essential to many processes in the human body so we absolutely need it to survive. What that iron needs though, is to be regulated. So how is iron regulated within the body? The "CUre" in the form of the element CU, otherwise known as copper. So again, why beef liver? Well it just so happens to be the most concentrated source of copper on the planet.

The first clue that I will present to you that tells us how copper can work to regulate iron in the body comes from a study done by Leslie Klevay, a prominent copper researcher in 2001 which showed that high iron increased the dietary copper requirement of the animals studied. Furthermore, it concluded that people with iron overload may benefit from copper supplementation, particularly if they habitually consume a diet low in copper. Another study by Klevay in 2011 showed that at least a quarter of adults consume less than the recommended daily average in the USA and Canada. Andrea Chambers et al. in a study done on copper intake and deficiency further showed that the optimal intake was actually 2.6mg Cu/d in contrast the the USA recommended daily average of 0.9mg Cu/d (2010). This is alarming because if one quarter of adults aren’t consuming 0.9mg per day, then you can bet that a lot less are consuming 2.6mg a day. This means first and foremost that a vast number of people have suboptimal levels of copper in their system.

So there are some clues in the studies above that show that iron regulation is dependent on copper, but a 2010 nutritional review titled “Metabolic crossroads of iron and copper” by James F Collins, Joseph R Prohaska, and Mitchell D Knutson definitively shows this connection. When dietary copper is absorbed, it is transported by albumin or a2-macroglobulin to the liver, where it is incorporated into a protein called ceruloplasmin (CP) or excreted into bile. It is important to keep in mind that 95% of total plasma copper is found in ceruloplasmin, so any process that is ceruloplasmin dependent is copper dependent. CP functions to deliver copper to other organs/tissues and is important for iron release from certain tissues.


Figure 1

Overview of whole body iron and copper homeostasis, highlighting points of interaction (James F Collins, Joseph R Prohaska, and Mitchell D Knutson, 2010)

Here are some important interactions that copper has in relation to iron:

  • Iron gets delivered to bone marrow for red cell hemoglobin production, and iron utilization by these cells is copper dependent.
  • Iron is taken up by other tissues, including the brain, where iron release is dependent on GPI-CP (glycosylphosphatidylinositol-linked ceruloplasmin). Again CP is 95% copper.
  • Iron contained within erythrocytes eventually is recycled by reticuloendothelial (RE) macrophages where it can be stored until times of need. The release of iron from RE macrophages is a copper dependent process, again involving CP and GPI-CP.
  • The absence of CP leads to iron accumulation in the pancreas, retina, and brain, which means that CP is critical for iron homeostasis (Xu et al., 2004)
  • Liver copper levels vary inversely according to iron status, so this means high iron in the liver means low copper and vice versa.

Pt. 1 showed how detrimental it is to have iron overloading the body, sitting in our tissues. This evidence clearly shows that copper is critical in order for iron to move out of the tissues and be utilized. To recap, when iron becomes trapped in our tissues it leads to a loss of mitochondrial respiration, and subsequently to disease. This is caused by oxidative stress in the form of oxygen leakage, known as reactive oxygen species (ROS) e.g. hydrogen peroxide. Copper salts have been shown to stimulate peroxide decomposition (Gutteridge, 1977; Sree Kumar et. al, 1978). This is very important because hydrogen peroxide or ROS is what conspires with iron to damage the mitochondria (Turrens et. Al, 1985), so copper therefore helps stop ROS from causing disease. Not only is copper important for stopping oxidation, but according to C.J.A. Van Den Hamer and G. Buyze, ceruloplasmin is the only oxidase in human serum, and since 90-95% of serum copper is tightly bound in ceruloplasmin, this means that copper is the only mineral that plays a process in catalyzing oxidation reduction reactions within the blood (1965). Reducing oxidation means reducing disease.

In terms of specific diseases that are caused by copper deficiency, there is a 2018 study by James J DiNicolantonio, Dennis Mangan, and James H O’Keefe that shows a link between copper deficiency and ischaemic heart disease. They note that low dietary copper intake reduces immune response, and it is not restored to normal levels even after several weeks of high copper intake. They also note that copper may exert a protective effect against iron induced oxidation, and most importantly, that normally benign levels of body iron may increase heart disease risk factors in the face of copper deficiency. In a 2019 study by Lei et al., it was shown that copper deficiency in the serum or liver occurs in a wide range of liver diseases, and that a notable clinical feature of these diseases included iron overload.

So we now know that iron overload causes a multitude of chronic diseases, and copper is the key to moving the iron out of the tissues to prevent the problems that stem from that. So why beef liver? Can’t we just supplement copper and be done with it? If you only went by the evidence presented in Pt. 1 and 2, then it would make sense to get a copper supplement and the problem is solved. There is one missing piece however. To illustrate this point, think of your body as a house: iron are the bricks, and copper is the construction worker laying those bricks where need be. Copper needs to get to the construction site though, and it can’t do it alone. In order to get to the construction site, it needs transportation, a bus, if you will. That bus that takes copper to work is retinol, otherwise known as Vitamin A. In Pt. 3 I will go into detail on Vitamin A and its relationship to Copper. So let's go back to the original question, why beef liver? Well, beef liver happens to have extremely high concentrations of Vitamin A, and copper, as well as some iron in very favourable ratios so you don’t have to buy multiple supplements and hope that the ratio works. Nature has done this job for us! Therefore incorporating this food will help enable efficient energy production at a cellular level, which is the universal requirement for a human being to thrive.

As a footnote, I wanted to write a special thanks to Morley Robbins and his book Cure Your Fatigue as well as the resources on his website If it weren’t for the research that he has been doing for years, I would have truly not known where to start on this article and probably wouldn’t have started Nutrimal as a whole. His work on the relationship between copper and iron, in addition to other topics such as magnesium, soil depletion, among other things has taught me so much about how to create health at the root rather than the allopathic way of chasing and relieving symptoms. Hopefully he sees my work one day and I get to tell him that directly.


  1. Klevay LM. Iron overload can induce mild copper deficiency. J Trace Elem Med Biol. 2001;14(4):237-240. doi:10.1016/S0946-672X(01)80009-2
  2. Klevay LM. Is the Western diet adequate in copper?. J Trace Elem Med Biol. 2011;25(4):204-212. doi:10.1016/j.jtemb.2011.08.146
  3. Chambers A, Krewski D, Birkett N, et al. An exposure-response curve for copper excess and deficiency. J Toxicol Environ Health B Crit Rev. 2010;13(7-8):546-578. doi:10.1080/10937404.2010.538657
  4. Collins JF, Prohaska JR, Knutson MD. Metabolic crossroads of iron and copper. Nutr Rev. 2010;68(3):133-147. doi:10.1111/j.1753-4887.2010.00271.x
  5. Van Den Hamer CJA, Buyze G. The Determination of Ceruloplasmin. Published 1965. 
  6. Xu X, Pin S, Gathinji M, Fuchs R, Harris ZL. Aceruloplasminemia: an inherited neurodegenerative disease with impairment of iron homeostasis. Ann N Y Acad Sci. 2004;1012:299-305. doi:10.1196/annals.1306.024
  7. Gutteridge, J. M. C. (1977) Biochem. Biophys. Res. Commun. 77, 379-386
  8. Sree Kumar, K., Rowse, C. & Hochstein, P. (1978) Biochem. Biophys. Res. Commun. 83, 587-592 
  9. Turrens JF, Alexandre A, Lehninger AL. Ubisemiquinone is the electron donor for superoxide formation by complex III of heart mitochondria. Arch Biochem Biophys. 1985;237(2):408-414. doi:10.1016/0003-9861(85)90293-0
  10. DiNicolantonio JJ, Mangan D, O'Keefe JH. Copper deficiency may be a leading cause of ischaemic heart disease. Open Heart. 2018;5(2):e000784. Published 2018 Oct 8. doi:10.1136/openhrt-2018-000784
  11. Yu L, Liou IW, Biggins SW, et al. Copper Deficiency in Liver Diseases: A Case Series and Pathophysiological Considerations. Hepatol Commun. 2019;3(8):1159-1165. Published 2019 Jun 26. doi:10.1002/hep4.1393

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